CCL3 (C-C Motif Chemokine Ligand 3)

Comprehensive single-cell analysis identified selective chemokine recruitment signatures supporting γδ T-cell infiltration but revealed paradoxical corecruitment of immunosuppressive populations. Patient stratification through chemokine profiling, combined with γδ T-cell enrichment and targeted chemokine antagonism, represents a rational therapeutic strategy.

leverage a newly developed neutrophil analysis framework to identify CCL3 as a conserved marker for tumor-associated neutrophils (TANs) across human and murine cancers. Using complementary genetic manipulation strategies, they demonstrate that neutrophil-derived CCL3 supports pro-tumor TAN survival within hypoxic tumor niches.

The decrease of CXCL9 and CXCL10 correlated with greater kidney function recovery at one-year follow-up. These molecules could serve as noninvasive biomarkers and may aid fine patient monitoring.

Through mechanistic perturbations of neutrophil-derived CCL3 in mice, we show that it sustains TAN survival in hypoxic tumor regions via CCR1-dependent signaling. These findings establish CCL3 as a conserved marker and functional driver of pro-tumor neutrophils in growing tumors, and provide a scalable framework for dissecting neutrophil biology across cancer types.

Mulitple molecular mechanisms involved in oral cancer management with shikonin have been elucidated providing a glimpse og the underlying therapeutic targets for the disease.

No single marker provides sufficient accuracy across all healing phases, highlighting the need for multimodal approaches that combine morphological assessment with panels of temporally complementary biomarkers. Standardization of methods and additional high-quality human studies are essential to improve the reliability and forensic applicability of wound age estimation.

The combination of rosuvastatin and bortezomib exerts a synergistic effect by inhibiting CCL3, thereby rebalancing bone remodeling and promoting osteogenesis. This strategy represents a promising novel therapeutic approach for mitigating MBD.

P4, N=78, Not yet recruiting, Wake Forest University Health Sciences | Trial completion date: Dec 2030 --> Aug 2028 | Trial primary completion date: Dec 2028 --> Jul 2028

This study defines a spatially organized stromal-immune signaling axis that drives immune exclusion and immunotherapy resistance in ccRCC. Targeting the POSTN⁺ CAF-CCL3⁺ macrophage interaction offers a promising strategy to remodel the fibrotic barrier and restore antitumor immunity.

These findings suggest that lutein reprograms M2 macrophages toward an M1-like phenotype and disrupts tumor-promoting signaling within the TNBC microenvironment, highlighting its potential as an adjunct therapeutic agent.

The CYTOscore based on IL-8, CCL3, and CCL4 effectively predicts treatment response and survival in ESCC patients receiving CRT plus anti-PD-1 antibody.

Nf1 OPG mice were treated with standard of care (SOC; carboplatin), clinically evaluated (everolimus, mirdametinib), and investigational (pexidartinib, HBS-101, lamotrigine) drugs during the period of most rapid tumor growth (6-12 weeks of age). This referential preclinical study design affords direct head-to-head comparisons of investigational therapies relative to SOC treatment using clinically meaningful outcomes (OPG growth and RNFL thickness). Using this strategy, lamotrigine emerged as the most promising therapy for limiting tumor progression and vision loss in Nf1-OPG mice, relevant to clinical translation for children with NF1-OPG.